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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4466_Библиотеки_им_академика_М_И_Перельмана
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Otitis Media withEffusion andHearing
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Loss inChildren
MuratKar, NurayBayar Muluk, andHeshamNegm
17.1 Introduction
Otitis media with effusion (OME), a term also encompassing serous otitis media, is
a condition in which uid accumulates in the middle ear, but there are no indications
of an acute infection [1]. There is also a subgroup of cases of OME where the uid
is viscous and yellow in colour and has the consistency of glue when viewed during
tympanic surgery [2]. This condition is termed ‘glue ear’. Although OME and glue
ear are sometimes used interchangeably, glue ear in fact only occurs in a portion of
cases of OME [3].
The effusion in OME does not contain pus. It is mucoid or serous. The usual
presenting symptoms are auditory impairment or feeling the ear is full, whilst
pyrexia or otalgia rarely occur. In paediatric cases, auditory impairment is usually
no more than mild, being revealed by audiogram rather than spontaneously reported.
Serous otitis media involves the formation of a watery and clear effusion as a
result of transudation caused by negative pressure developing in the middle ear
space [4]. It is a subtype of OME.
17
M. Kar (*)
Alanya Training and Research Hospital, Alanya Alaaddin Keykubat University, Antalya,
Türkiye
e-mail: drmuratkar@gmail.com
N. Bayar Muluk
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, Türkiye
e-mail: nbayarmuluk@yahoo.com
H. Negm
Department of Otorhinolaryngology, Faculty of Medicine, Cairo University, Cairo, Egypt
e-mail: drnegment@hotmail.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_17
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It is important for clinicians to appreciate that there are signicant differences
between OME and other infective conditions affecting the middle ear cavity [5].
The term ‘otitis media’ is a generalised term for any inammatory condition of the
middle ear. It does not indicate the particular cause or pathological mechanism
involved. The pneumatised regions of the temporal bone (mastoid, perilabyrinthine
and petrous apex air cells) are interconnected; hence, otitis media may lead to
inammation of these spaces, too. A range of disorders are all grouped under the
umbrella term otitis media, namely, acute otitis media (AOM), recurrent acute otitis
media (RAOM), OME and chronic otitis media with effusion (COME) [6].
M. Kar et al.
17.2 Pathophysiology
OME may develop following AOM, as it begins to resolve and the acute phase has
passed. Up to 45% of paediatric cases of AOM still have an effusion present 1
month after onset, with this number falling to 10% at the 3 month mark [6].
17.2.1 Classical Explanation
There are two principal ways in which the pathogenesis of AOM is said to occur.
According to the classical theory, the auditory tube does not function correctly,
which is a necessary step in pathogenesis. The auditory tube is generally credited
with three functions, namely, equalising the pressure in the middle ear cavity and
external auditory meatus, draining secretions and defence of the middle ear. If these
functions are impaired, AOM may develop. Accordingly, several events may trigger
eventual AOM, ranging from anatomical abnormality causing obstruction, to allergic inammation, an infection of the upper respiratory tract or traumatic injury [6].
In cases where the auditory tube is dysfunctional for more than a brief period, the
pressure in the middle ear cavity will fall, since nitrogen and oxygen diffuse out of
this space. If there is a sizeable pressure gradient as a result, transudation develops
from the mucosa, with a serous, typically sterile, uid building up in the space.
Since there is no drainage through the auditory tube, this stagnant uid provides a
suitable environment for bacterial species to grow, and AOM develops in response.
However, this theory cannot be entirely correct, since it has been shown several
times that cases of AOM and OME feature identical bacterial pathogens [4].
17.2.2 More Recent Explanations
More recently, it has been proposed that the initiating event in AOM is mucosal
inammation within the middle ear in response to pre-existing bacteria in the cavity.
Imaging studies were used by Bluestone etal. to demonstrate reux passing into the
auditory tube in paediatric cases of recurrent otitis media [7]. Moreover, pepsin has
been identied in the middle ear cavity of some 60% of paediatric OME cases [8],
17 Otitis Media withEusion andHearing Loss inChildren
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albeit reux into the auditory tube can also be observed in individuals without any
evidence of disease.
Likewise, O’Reilly etal. discovered, in their study of 129 children undergoing
myringotomy with grommet insertion for an indication of otitis media, that pepsin
A was present in aspirates from 64 cases. The presence of pepsin A indicated that
stomach contents must have been reuxed as far as the nasopharyngeal region.
These researchers relate this nding to the development of AOM by suggesting
reux triggers an inammatory response or worsens any inammatory response that
is already occurring [9].
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17.2.3 Middle Ear Effusion
Whatever the causative agent is in cases of AOM, a dysfunctional auditory tube is
virtually invariably present in cases of OME.In animal models, when the auditory
tubes are experimentally ligated, a long-standing effusion develops in the middle
ear. Even when the infection has been eradicated and inammatory responses cease,
the effusion continues to be present due to non-drainage of the middle ear. The
inability to drain the effusion may be a result of various pathophysiological changes,
such as non-functioning cilia, oedema within the mucosa, excessive viscosity of the
uid and, potentially, pressure changes in the middle ear [6].
Not all cases of AOM proceed to become OME. There have been proposed a
variety of mechanisms to account for how an effusion develops in the cavity. One is
that inammation of the mucosal lining causes uid to be secreted. According to
this explanation, the mucosa undergoes sensitisation following the presence of bacterial pathogens, and when reux occurs from time to time, bacterial antigens are
present to trigger an inammatory response. However, as explained earlier, the bacterial species detected in cases of OME do not differ from those present in AOM.The
effusion is not completely void of pathogens, as used to be thought [6].
17.2.4 Cleft Palate
In paediatric cases of cleft palate, OME is always seen. This is explained as occurring due to the incorrect insertion of the tensor veli palatini muscle. Accordingly,
when patients swallow or open their mouths wide, this muscle does not perform its
usual function of opening the auditory tube. Thus, the tune is functionally
blocked [10].
17.3 Frequently Occurring Pathogens
The bacterial pathogens that are most frequent in cases of AOM are Streptococcus
pneumoniae, followed by Haemophilus inuenzae and then Moraxella catarrhalis.
The same group of organisms are also the most common bacterial causes of sinusitis
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and pneumonia. These three species collectively are found in 85% of cases of
AOM.They occur with the following frequency [6]:
• S. pneumoniae is present 35% of the time, with no apparent effect of age on
prevalence. The most frequently identied serotype is 19, followed by 23, 6,
14 and 3.
• Some 20% of cases are attributed to H. inuenzae. At present, between 25 and
45% of the organisms isolated are capable of expressing a beta-lactamase, and
the frequency of antibiotic insensitivity is clearly rising.
• In cases of AOM, M. catarrhalis is responsible for between 4 and 13%. This
gure rises during the winter and autumn months. Beta-lactamase expression
occurs in 70–100% of these pathogens.
The other pathogenic bacteria involved are Streptococcus pyogenes,
Staphylococcus aureus, enteric bacteria-staining Gram-negative, and anaerobic species. Pseudomonas is the most commonly isolated bacterial genus in cases where an
effusion has persisted for more than 3months.
No pathogen is identied in 30% of aspirates obtained during tympanocentesis.
A meta-analysis based on ten studies dating from 30years ago collated data on 663
patients. In 29 cases (4.4%), a viral pathogen was identied. Data from more recent
research indicate that a viral pathogen is identiable in 15–20% of cases of AOM,
co-existing with a bacterial pathogen. The viral pathogens most common in such
cases are respiratory syncytial virus (RSV) and inuenza virus [6].
M. Kar et al.
17.4 Risk Factors
A number of risk factors for OME have been identied. These include the environment, age and dysfunction of the auditory tube [6].
17.4.1 Environment
There are a number of factors in the environment of the patient that increase the risk
of OME, besides the presence of specic pathogens. Epidemiological data indicate
the following are associated with raised risk: bottle feeding, being fed lying down,
having a brother or sister with a middle ear infection, going to a childcare facility,
being allergic to frequently encountered environmental allergens, low socioeconomic condition, presence of smokers in the household and a family history of
OME in at least one parent [11, 12].
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17.4.2 Age
Age is strongly associated with a heightened risk of OME.During infancy, the auditory tube in the anatomical position is virtually parallel to the ground, with the angle
steadily increasing up to adulthood, when it has an angle of 45°. Furthermore, the
anatomical conguration of the auditory tube in neonates permits less efcient ventilation of the middle ear than in adults [6, 13].
The results of several Danish studies on paediatric cases show that, up to the age
of 1year, in 24% of ears assessed, a type B (at) or type C (indicating negative pressure) was found on tympanometry. Auditory function became more normal in
springtime or the summer months, but winter witnessed declining function. The
peak occurrence of a type B pattern was between the ages of 2 and 4 years.
Thereafter, this type of tympanogram is more rarely seen, as could be anticipated
from the lower frequency of OME in children after the age of 6years [6].
It is vital that OME affecting one ear in an adult is identied without delay as the
most dangerous underlying diagnosis is a neoplasm of the nasopharynx [6].
17.4.3 Disrupted Auditory Tube Function
OME is also more common in cases where the nasopharyngeal ostium cannot
remain patent. This situation frequently affects individuals with cleft palate or
Down Syndrome, as well as other conditions involving the palatal region. It has
been proposed that the reason patients with cystic brosis are more prone to OME
is because the clearance of accumulated mucus by ciliary action is impaired in cystic brosis, where mucus is abnormally viscid [6].
17.4.4 Diet
Research undertaken by Choi etal. concluded that eating a diet overly rich in fats
does increase the risk of paediatric OME, although several other aspects of diet
examined did not affect the risk, namely, body mass index and classication, dietary
protein, water or sodium, and the times at which carbohydrates were consumed [14].
17.4.5 Other Factors
Kaya and colleagues disagree with the ndings of the research by Choi etal. These
authors state that OME is indeed linked to the patient’s being overweight or obese,
based on a sample of 60 paediatric cases of OME and 86 healthy controls, with an
age range of 2–10years. They examined data linking body mass and height, noting
that there was an association between excess body weight (including obesity) and
higher frequency of OME. They speculate that being overweight or obese
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potentially increases the risk of OME, or, conversely, that OME is a risk factor for
obesity [15].
Walker and colleagues noted specic characteristics of paediatric cases of OME
occurring prior to school age [16]. These patients typically have a blocked nose,
snore frequently or invariably, spend an above average length of time in childcare
facilities each week, have coryzal illnesses frequently, tend to have siblings in whom
grommet placement has already occurred, were born following prolonged labour
and began drinking bovine milk relatively early. Being of Asian extraction and having older siblings, in contrast, had an association with less likelihood of developing
OME [16].
M. Kar et al.
17.5 Epidemiological Features
Acute otitis media occurs once or more in the majority of children, that is, in
84–93%. Moreover, around four in ve children experience OME at least once by
the time they are 10years old. The cross-sectional prevalence of auditory impairment secondary to OME of at least 3-month duration is 5% in children aged between
2 and 4years. The peak prevalence of OME occurs up to the third birthday and falls
rapidly after the sixth birthday [6].
17.6 OME andAuditory Impairment
The aims in managing cases of OME are to remove the effusion from the middle ear
cavity and normalise the pressure gradient, to restore auditory function. The rstline treatment consists of either watchful waiting or grommet insertion, which may
sometimes be accompanied by removal of the adenoids. Myringotomy without
grommet placement is not an effective option for treating OME.Initial results from
balloon dilatation of the auditory tube have been encouraging, but the method needs
further quantication of its benets and risks before it can be generally recommended [3].
The method chosen and the timing of any intervention may be decided by considering whether there are other co-existent problems that may worsen the effect of conductive-type auditory impairment, such as speech and language disorders or learning
disability. It is also important to consider how severely impaired hearing is, how long
the effusion has been present and if the lesion is one- or two-sided [1, 2]. The season
in which OME occurs also inuences the outcome, with summer and autumn episodes less likely to resolve without intervention [1, 17, 18]. With these factors taken
into consideration, the two options of observing and intervening only when required,
or performing myringotomy with grommet insertion, remain valid for most cases.
Hearing aids, whether external or implanted, are appropriate only in paediatric
cases of persistent OME where the insertion of grommets is unfeasible or where it
brings no benet, such as in cases of aural atresia or abnormally functioning ossicles [3].
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Children in whom there is a risk of problems with speech and language
development, or learning are a special category within OME clinical management. This group encompasses children with pre-existing auditory impairment,
inherited disorders (Down Syndrome, 22q11.2 deletion disorder) or neurodevelopmental conditions (such as autism), abnormal craniofacial development (such as
cleft palate) and those with visual problems not corrected by appliances, since these
children are especially reliant on hearing to compensate for their lack of vision
[1, 2, 19].
Thus, assessment of hearing should be carried out on children with OME falling
in the ‘at risk’ category [1]. The conductive-type auditory impairment found in
OME has a disproportionately negative effect on disabled patients. The modality
used to assess auditory function should be selected according to how old the child
is and how much he or she has the ability and willingness to co-operate. Where
auditory loss is large, operative intervention is indicated. Patients in whom language development is delayed need to be assessed by a speech and language
pathologist.
There is consensus amongst various professional bodies that children diagnosed
with OME and who have a speech and language or learning disability require surgical consultation at an early stage, namely, no later than 3 months after diagnosis [1,
19]. In the majority of trials where the outcomes of OME were examined, whether
immediate or longer term, such cases have been purposely excluded [20]. Thus,
there is a lack of denite evidence to quantify the extent to which these individuals
suffer more severe consequences. Practical experience, however, suggests that conductive auditory impairment can only worsen the prognosis where a pre-existing
linguistic or intellectual disability is present [21].
Children without pre-existing linguistic or intellectual disabilities. For paediatric patients without these risk factors, the usual practice is to assess auditory
function only where OME is persistent and the duration exceeds 3 months [1, 19].
The advantage of this delay is that the auditory impairment has often already spontaneously remitted by this point [2]. There may be an additional need for speech and
language pathology appraisal of a case, especially if the auditory impairment is
evident at a threshold of 21dB or more.
Managing patients who do not fall into the special risk category depends on
judgements about how the eardrum and middle ear cavity appear, the results of auditory testing (including audiometric and tympanometric evaluation), how long an
effusion has been present, whether one ear or both is affected, and the wishes of
parents or other carers [3].
Structural changes affecting the ear drum or middle ear. The following are
signs that an urgent referral for surgical intervention is required: atelectasis of the
tympanic membrane (i.e. retraction); partial collapse of the drum/retraction pocket,
a perforated eardrum, discharge from the ear, and cholesteatoma [1]. In these cases,
surgical intervention may be needed for another indication, besides OME.
The threshold for hearing is 40dB or higher. Children with OME-induced
auditory impairment raising the threshold for hearing to 40 dB or above should
receive a referral for surgical assessment.
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M. Kar et al.
Despite the paucity of evidence about longer-term outcomes in paediatric patients
with this degree of impairment, if the loss becomes longstanding, there may be
negative effects on the development of speech and language and scholastic achievement. Thus, an ENT assessment is warranted [22–24].
A systematic review has examined the benets of grommet insertion on auditory
perception. The trials reviewed all involved paediatric patients with OME.The procedure seems to offer limited benet, and by 6–9months post-surgery, any benet
appears minimal. This is the normal time frame for the condition to resolve spontaneously [20]. No benet in terms of speech or language acquisition, nor intellectual
development, was proven, albeit the evidence base consulted was slender. There is
a lack of published evidence regarding paediatric patients in whom a pre-existing
decit of speech, linguistic performance, psychological development or intellect is
present [3].
Hearing threshold located between 21 and 39dB. In children without preexisting disability who experience auditory impairment sufcient to raise the hearing threshold to between 21 and 39dB as a result of OME, a more conservative
approach is suitable. Since the degree of auditory impairment is mild, decisions may
be taken on the basis of a risk-benet discussion with parents or carers about watchful waiting or grommet insertion [1, 2]. The majority of patients in this situation do
not require surgical intervention, and watchful waiting is adequate management.
The general recommendation is to rebook the patient and arrange further hearing
tests after between 3 and 6months [3].
The extent to which benet outweighs the risks of surgery can usually be decided
by considering how the child would be affected by having a mild auditory impairment lasting 6–9months. This is the period for which grommet insertion has been
shown to be benecial. Nonetheless, even when various studies conducted in this
area, including some RCTs and other studies using controls, have been systematically reviewed, the evidence base supporting the benets on speech and linguistic
performance of grommet insertion for children with mild auditory decits appears
weak [20, 25–27]. Grommet insertion is potentially justied in children with OME
affecting one or both ears, which has persisted for at least 3 months (i.e. it qualies
as chronic), and impacts scholastic achievement and creates challenging behaviour
or lowers the quality of life [19].
A number of factors need to be taken into consideration when deciding, such
as the following [1, 2, 19, 28]
• Is language abnormal or delayed, if the child is very young? Is scholastic achieve-
ment impacted by an older child’s acting out-of-character?
• Is OME chronic (has lasted at least 3months) and affecting both ears? Research
employing an observational design has determined that OME affecting both ears
tends to cause a higher degree of severity in auditory impairment and to resolve
more slowly than unilateral cases. After 6 months only around 25% of cases
remit spontaneously, whilst this gure is 30% at 1 year [1, 2, 29].
• Is OME of at least 3 months’ duration (i.e. chronic), whether affecting one or
both ears, whilst also being the most probable cause of any of the following
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issues: difculty balancing (from vestibular involvement), scholastic under-
achievement, challenging behaviours, otalgia, and a poorer quality of life than
usual, from the point of view of parents or carers? This change in life quality may
be manifested as insomnia or acting out-of-character [30–32].
• An extended period for which OME persists, such as OME affecting one ear
which persists for at least 6months, or which has been present for a minimum of
6months in the preceding year, makes the lesion less likely to resolve spontane-
ously [33] and entails greater likelihood that the eardrum will be structurally
damaged [24].
If there is no auditory impairment present (in other words, any loss of hearing
occurs at a level of 20dB or less), and speech, language and development are all on
target, the patient may be followed-up by watchful waiting. Since auditory testing
usually occurs 3 months after the onset of OME, this means watchful waiting lasts
for 6 months in total [1, 2].
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17.7 Clinical Work-Up
Probably, the diagnostic test most value in assessing a case of OME is tympanometry. Some 43% of tympanometric tests in patients with OME are of type B, with
47% of type C, showing the middle ear pressure is lowered. The effusion may be
aspirated by performing tympanocentesis, which may be satisfactorily performed in
clinic, even if the patient is very young. Performing tympanocentesis allows culture
of the aspirate and is therapeutic in its own right [34].
However, to obtain the gold standard diagnostic evidence to show OME, myringotomy is needed. This procedure benets from a greater degree of exposure of the
lesion and allows more effective suctioning than is possible through tympanocentesis [35].
Imaging using computed tomography (CT) plays a signicant role in excluding
potential complications of otitis media, such as mastoiditis, thrombus formation in
the sigmoid sinus or where the lesion may erode into the bone and spread intracranially. It is also valuable if there is an atypical cause, such as cholesteatoma. CT is
especially benecial in cases of OME affecting one side only and in which a suspected mass may be present in the nasopharynx or auditory tube [6].
Magnetic resonance imaging (MRI) has particular value in cases where a mass
lesion within the soft tissues is potentially aggravating a middle ear effusion. MRI is
especially good at dening the boundary between different soft tissues and can show
how far a mass, in the nasopharynx, for example, has invaded into the cranial cavity.
MRI can also easily reveal particular vascular complications, for example, thrombosis within the venous sinuses. For these purposes, the augmented MRI techniques,
such as magnetic resonance venography (MRV) and magnetic resonance arteriography (MRA) are helpful. In all cases where the lesion extends into the cranial cavity,
nonetheless, CT is necessary to dene the osseous anatomy and determine the path
the lesion has taken, whether via the nasopharynx or the temporal bone [6].
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M. Kar et al.
17.8 Management
Pharmacotherapy for OME involves the use of antibiotics, corticosteroids, antihistamines, decongestant and mucolytic agents. This approach to treatment has, however, been criticised on the grounds of limited evidence for clinical benet in the
longer term, plus the cost and side effect burden involved. In particular, the
International Federation of Otorhinolaryngological Societies Congress in 2017
looked at each class of agent and recommend against their use on the grounds outlined above [7].
In chronic OME, the treatment modality enjoying the broadest acceptance is
surgery, for the effectiveness of which there is clear evidence. Surgical options
include myringotomy (+/− grommet insertion), removal of the adenoids or a procedure involving all three. As rst-line therapy for OME, tonsillectomy has not been
demonstrated to offer signicant advantages [6].
17.8.1 Grommets
Possible indications: Before deciding to treat OME by grommet insertion, there
should be a discussion of the benets and risks involving the patient, parents or carers, GP and ENT specialist.
The following are possible situations where grommet placement is indicated [1,
2, 19]
• OME in a child who has risk factors for speech or language delay or learning
disability. This applies regardless of the degree of auditory impairment. It is rec-
ommended such cases are seen by an ENT specialist within 3 months.
• Alteration to the eardrum, such as a retraction pocket.
• Chronic auditory impairment as a result of OME resulting in an auditory thresh-
old of 40dB or above.
• OME in both ears that has persisted for at least 3 months, or in one ear for at least
6 months, or OME which has recurred within a year, resulting in a total duration
lasting at least 6months within a year.
References
1. Rosenfeld RM, Shin JJ, Schwartz SR, etal. Clinical practice guideline: otitis media with effusion (update). Otolaryngol Head Neck Surg. 2016;154:S1.
2. National Institute for Health and Care Excellence. Otitis media with effusion in under 12s:
surgery. www.nice.org.uk/nicemedia/pdf/CG60NICEguideline.pdf. Accessed 8 Nov 2012.
3. Pelton SI, Marom T.Otitis media with effusion (serous otitis media) in children: management.
In: Kaplan SL, Isaacson GC, Torchia MM, editors. . Waltham: UpToDate; 2021.
4. O'Connor SS, Coggins R, Gagnon L, Rosenfeld RM, Shin JJ, Walsh SA.Plain language summary: otitis media with effusion. Otolaryngol Head Neck Surg. 2016;154(2):215–25.
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